Absence of thrombospondin-2 causes age-related dilated cardiomyopathy
| Autor: | Swinnen, M., Vanhoutte, D., Van Almen, G., Hamdani, N., Schellings, M., D'hooge, J., Van Der Velden, J., Weaver, M., Sage, E., Bornstein, P., Verheyen, F., Chuah, Marinee, Westermann, D., Van De Werf, F., Schroen, B., Carmeliet, P., Pinto, Y., Heymans, S., VandenDriessche, Thierry |
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| Přispěvatelé: | Cell Biology and Histology, Division of Gene Therapy & Regenerative Medicine |
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Male
Mice Knockout Myocardium/pathology endocrine system Cardiomyopathy Dilated/pathology mice Myocarditis/etiology Myocardium/metabolism Thrombospondins/genetics fibrosis Gene Transfer Techniques Matrix Metalloproteinase 2/metabolism virus diseases Cardiomyopathy Dilated/etiology Myocytes Cardiac/metabolism UP-REGULATION Enzyme Activation cell death Thrombospondins/deficiency immune system diseases Cardiomyopathy Dilated/mortality Proto-Oncogene Proteins c-akt/metabolism Female Myocytes Cardiac/ultrastructure Cardiomyopathy Dilated/prevention & control |
| Popis: | BACKGROUND: The progressive shift from a young to an aged heart is characterized by alterations in the cardiac matrix. The present study investigated whether the matricellular protein thrombospondin-2 (TSP-2) may affect cardiac dimensions and function with physiological aging of the heart. METHODS AND RESULTS: TSP-2 knockout (KO) and wild-type mice were followed up to an age of 60 weeks. Survival rate, cardiac function, and morphology did not differ at a young age in TSP-2 KO compared with wild-type mice. However, >55% of the TSP-2 KO mice died between 24 and 60 weeks of age, whereas CONCLUSIONS: TSP-2 expression in the heart protects against age-dependent dilated cardiomyopathy. |
| Databáze: | OpenAIRE |
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